RESUMEN
Background: There is increasing evidence of cardiac involvement in SARS-COV-2 infections. This may not only apply to symptomatic infections but may also affect asymptomatic athletes. This study aimed to characterize the possible acute cardiac involvement of SARS-COV-2 infection in athletes both morphologically and functionally. Methods and results: Eight elite handball players (27±3.5 y) with past SARS-COV-2 infection were retrospectively analyzed and compared with four uninfected team-mates (22±2.6 y). Athletes were examined 19±7 d after positive PCR-test. Echocardiographic assessment of the global longitudinal strain under resting conditions was not significantly changed after SARS-CoV2 infection (-17.7% vs. -18.1%) but magnetic resonance imaging showed minor signs of acute inflammation/edema in all patients (T2-mapping: +4.1ms) without reaching the Lake-Louis criteria. Spiroergometric analysis showed a significant reduction in VO2max (-292 ml/min, -7.0%), oxygen-pulse (-2.4 ml/beat, -10.4%), and respiratory minute volume (VE) (-18.9 l/min, -13.8%) in athletes with a history of SARS-CoV2 infection (p<0.05, respectively). The parameters were unchanged in the control group. Conclusion: SARS-CoV2 infection caused functional impairment of cardiopulmonary performance primarily under stress in elite athletes. It seems reasonable to screen athletes after SARS-CoV2 infection at least with spiroergometry to mark performance limitations and to ensure an optimal return to competition.
RESUMEN
There is increasing evidence of cardiac involvement post-SARS-CoV-2 infections in symptomatic as well as in oligo- and asymptomatic athletes. This study aimed to characterize the possible early effects of SARS-CoV-2 infections on myocardial morphology and cardiopulmonary function in athletes. Eight male elite handball players (27 ± 3.5 y) with past SARS-CoV-2 infection were compared with four uninfected teammates (22 ± 2.6 y). Infected athletes were examined 19 ± 7 days after the first positive PCR test. Echocardiographic assessment of the global longitudinal strain under resting conditions was not significantly changed (- 17.7% vs. - 18.1%). However, magnetic resonance imaging showed minor signs of acute inflammation/oedema in all infected athletes (T2-mapping: + 4.1 ms, p = 0.034) without reaching the Lake-Louis criteria. Spiroergometric analysis showed a significant reduction in VO2max (- 292 ml/min, - 7.0%), oxygen pulse (- 2.4 ml/beat, - 10.4%), and respiratory minute volume (VE) (- 18.9 l/min, - 13.8%) in athletes with a history of SARS-CoV2 infection (p < 0.05, respectively). The parameters were unchanged in the uninfected teammates. SARS-CoV2 infection caused impairment of cardiopulmonary performance during physical effort in elite athletes. It seems reasonable to screen athletes after SARS-CoV2 infection with spiroergometry to identify performance limitations and to guide the return to competition.